Autism is a neurological disorder characterized by alterations in social interaction, language development, repetitive movements and patterns of behavior. Its prevalence has increased from 1 in 2,325 births prior to the 1980's to an alarming 1 in 101 births today (Blaylock et al., 2009, Curr. Med. Chem. 16:157-170). Autism is a very complex neurological disorder that does not follow strictly genetic or deterministic etiology (Lander et al., 1994, Science, 265:2037-48; Baron-Cohen et al., 2005, Science, 310:819-23; Santangelo et al., 2005, Am. J. Pharmacogenomic. 5:71-92). Accordingly, defining a role for metabolism in the pathogenesis of autism is important to developing an understanding of the disorder and providing an accurate diagnosis and patient management of the disease, because strictly genetic causes account for only approximately 10% of autism cases. Multiple candidate susceptibility genes have been identified, such as the serotonin transporter gene (5HTT), the GABA receptor β subunit (GABRB3), ubiquitin ligase 3 (UBE3A), wingless type MMTV integration site family member 2 (WNT2), and reelin (RELN) (Folstein et al., 2001, Nat. Rev. Genet. 2:943-955; Buxbaum et al., 2004, Mol. Psychiatry, 9:144-150; Devlin et al., 2005, Mol. Psych. 10:1110-1116). Despite the genetic diversity underlying mutations and patient symptoms (McCracken et al., 2002, N. Engl. J. Med. 347:314-321; Moore et al., 2004, Ann. Pharmacother. 38:1515-1519; Zhao et al., 2005, Intern. J. Neuroscience, 115:1183-1191) there seems to be a converging metabolic dysfunction across cases (Bryson et al., 1998, Mental Retard. Dev. Disabil. Res. Rev. 4:97-103; Betancur et al., 2002, Mol. Psychiatry, 7:67-71; Moore et al., 2004, Ann. Pharmacotherapy. 38:1515-19). Metabolism and metabolic alterations can play a significant role during neurodevelopment and autism pathogenesis (Pardo et al., 2007, Brain Pathol. 17:434-447). Thus, comparative studies to examine global biochemical differences between autistic and non-autistic brain can identify specific metabolic pathways that contribute to autism onset and progress. (Moore et al., 2004, Pharmacother. 38:1515-1519; Rasalam et al., 2005, Dev. Med. Child Neurol. 47 (8):551-555).